There is very good evidence that brain of aging animals and man have lowered amounts of functional catecholamine neurotransmitters. This apparently is the cause of movement disorders in the elderly as well as responsible for cessation of ovulation in females. We develop a hypothesis based on our preliminary studies and those of others that this may be caused by oxidative damage to brain membranes. We have found that catecholamines protect against oxidative damage to brain membranes; yet the presence of lipofuscin and neuromelanin, indicates that oxidative damage still occurs. We have found that in the tyrosinase catalyzed oxidation of catecholamines in the presence of membrane lipids, a free radical of apparently the catecholamine-lipid adduct is spin-trapped. Also in the oxidation of catecholamines to melanin products are produced which oxidatively attack membranes in a fashion resembling the potent neurotoxin, 6-hydroxydopamine (60HDA) which selectively kills dopaminergic neurons. We have also found that erythrosine-B (ERY-B) apparently in its free radical state oxidatively attacks membranes. We have proposed a series of experiments to understand killing and oxidative damage to brain membranes. We will test the hypothesis that hydroxyl free radicals produced in autooxidizing 60HDA, leads to neuron death via membrane lipid peroxidation. We propose experiments to understand during catecholamine oxidation the nature of its oxidation products with membranes. We propose experiments to understand the conditions necessary for brain membrane oxidation and determine if catecholamines act as natural protective compounds. Finally we plan a series of experiments to understand the mechanism of ERY-B mediated membrane oxidation.